Skin and soft tissue infections Flashcards

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1
Q

Clinical syndromes caused by staphylococcus aures

A
Folliculitis
Furuncles
Carbuncles
Impetigo
Cellulitis
Toxic shock syndrome
Post-operative wound infections
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2
Q

Clinical syndromes caused by streptococcus pyogenes

A
Impetigo
Erysipelas
Cellulitis
Necrotising fasciitis
Toxic shock syndrome
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3
Q

Impetigo

A
  • very superficial infection involving the epidermis
  • commonest in children and is usually on the face often around the mouth and nose
  • two forms
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4
Q

What are the two forms of impetigo?

A
  • non-bullous (‘honey-crust’) lesions, most commonly due to Strep pyogenes (Group A strep)
  • bullous, when bullae rupture they appear instead as thin ‘varnish’like’ crusts due to staph aureus
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5
Q

Folliculitis

A
  • infection of the hair follicles
  • may occur after exfoliation, use of a loofah sponge, shaving or spontaneously
  • whirlpool (hot tub or spa) folliculitis can be caused by pseudomonas aeruginosa
  • self-limiting so there is no specific treatment
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6
Q

Abcesses and furuncles

A
  • staph aureus is the leading community pathogen causing abcesses and furuncles
  • certain phage types are associated with recurrent episodes of furunculosis and may spread among family members
  • staphylococcal blood stream infection from a minor skin lesion or a furuncle may rarely result in severe complications, including osteomyelitis, septic arthritis and endocarditis
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7
Q

What’s an abcess?

A

A collection of pus in any tissue

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8
Q

What’s a furuncle?

A

An abcess in the skin, commonly called a boil

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9
Q

What’s a carbuncle?

A

Larger abcesses, interconnected furuncles

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10
Q

What is cellulitis and what are the 3 categories?

A

Acute spreading inflammation involving soft tissues but excluding muscle.

  • Erysipelas
  • Acute cellulitis
  • Necrotising fasciitis
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11
Q

Erysipelas

A
  • involve the superficial dermis
  • extremes of age
  • usually Group A strep (but can be group G, B, C)
  • face and leg commonest sites
  • distinction from acute cellulitis is unimportant clinically
  • blood cultures, aspirates, biopsies are usually negative
  • may recur in the same area (possibly related to local lymphatic insufficiency)
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12
Q

Treatment of erysipelas

A
Benzyl penicillin (iv)
High does iv flucloxacillin will cover both strep and staph infection if doubt about aetiology
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13
Q

Acute cellulitis

A
  • ‘wild fire’ onset
  • often high fever then cellulitis 12 hours later
  • rapidly spreading inflammation of the deep dermis and subcutaneous fat.
  • often subtle portal of entry
  • usually group A strep (sometimes staph aureus)
  • redness and pain, systemic signs and symptoms
  • lymphangitis can occur (streak of redness on lymphatics)
  • blood cultures/aspirates usually negative unless there is a purulent collection
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14
Q

Necrotising fasciitis

A
  • life threating
  • involves superficial fascia and underlying fat
  • two main bacterial causes: strep pyogenes and synergistic infections with anaerobic organisms mixed with aerobes (abdo surgery or perineal infection/trauma)
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15
Q

When would you suspect necrotising fasciitis instead of cellulitis?

A
  • nec fasc failure to respond to antibiotics
  • marked pain
  • very unwell
  • in mixed infection there could be crepitus or a foul smell
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16
Q

What’s fourniers gangrene?

A

A form of necrotising fasciitis affecting the male genitalia

17
Q

Diagnosis and treatment of necrotising fasciitis

A
  • Surgical exploration and debridement
  • antibiotic therapy can be guided by initial gram stain of debrided sufgical material and then culture results
  • if Strep nec fasc: high dose IV penicillin and clindamycin
  • if treating blind or mixed infection: iv cefuroxime, clindamycin and metronidazole
18
Q

Clinical definition of toxic shock syndrome

A
  1. temperature > 38.9
  2. systolic BP < 90mmHg
  3. rash with subsequent desquamation, especially on palms and soles
  4. involvement of three or more systems:
    - GI (vomiting, profuse diarrhoea)
    - muscular (severe myalgias or CPK 5x normal)
    - renal (creatinine twice normal with pyuria)
    - liver (hepatitis: bilirubin AST, ALT twice normal)
    - blood (thrombocytopenia <100000 mm^3)
    - CNS (disorientation without focal neurological signs)
19
Q

Gas gangrene

A

Clostridial myonecrosis

  • a necrotising gas forming process of muscle associated with systemic signs of toxaemia
  • approx 80% due to clostridium perfringens type A. Other causes: Clostridium novyi, Clostridium spticum
  • alpha toxin (lecithinase) is major toxin
  • myonecrosis, shock, haemolysis
  • usually related to trauma (can be minor), post-op (abdo), post partum, septic abortion
  • can also appear spontaneously often associated with an underlying colonic carcinoma or intra-abdominal abscess
20
Q

Treatment of gas gangrene

A

Emergency surgical debridement
Antibiotics
Hyperbaric oxygen

21
Q

Pathophysiology of tetanus

A
  • clostridium enters the body through a wound
  • spores germinate in anaerobic conditions
  • toxins are produced and disseminated through blood and lymphatics
  • toxins act at various sites in the NS including the peripheral end plate, spinal cord, brain, and sympathetic NS.
  • toxins gain access to the CNS via retrograde axonal transport in motor nerves
  • toxins move into the presynaptic inhibitory interneurons with resulting inhibition of release of inhibitory neurotransmitters (GABA in the brain, glycine in the spinal cord)
  • this results in heightened muscular activity
  • loss of glycine inhibition occurs in the intermediolateral grey matter of the spinal cord results in increased sympathetic activity
  • reduction of release of acetylcholine from motor neurons may result in paralysis of cranial nerves in cephalic tetanus
22
Q

Three forms of tetanus

A

Generalised
Local
Neonatal

In the generalised from the cervical, facial and masticatory muscles are affected first. There is then dysphagia, then generalised weakness, trismus and back spasm (opisthotonus)

23
Q

Clostridium tetani

A
  • in soil and GI tract of animals and humans
  • slender, motile, gram positive, anaerobic rod that may develop a terminal spore giving it a drumstick appearance
  • insensitive to heat
  • cannot survive in the presence of oxygen
24
Q

Clinical features of tetanus

A
  • the earliest manifestation of generalized tetanus are rigidity of the masseter muscle (lockjaw/trismus), and facial muscles, with straightening of the upper lip (grimace/risus sardonicus)
  • soon followed by rigidity of axial muscles with prominent involvement of the neck and back muscles (opisthotonus)
  • rigidity of axial muscles may precede or accompany trismus
  • stiffness of limb muscles may be evident with sparing of distal muscles
  • dysphagia and laryngospasm (asphyxiation) due to muscles involved
25
Q

Diagnosis of tetanus

A

clinical and EMG studies

26
Q

Treatment

A
Supportive (ICU)
Benzodiazepines
Debridement of wounds
Benzylpenicillin
Tetanus IVIg
27
Q

Organisms that might colonise venous ulcers

A
Staph aureus
Gram negatives (pseudomonas)
28
Q

When would you give someone with a venous ulcer antibiotics?

A

Cellulitis
Lymphangitis
Systemic infection

29
Q

Common cause of malignant otitis externa in diabetics

A

Pseudomonas

30
Q

Cause of athletes foot

A

Tinea pedis

31
Q

Onychomycosis

A

Fungal nail infection

32
Q

Treatment of fungal nail infections

A

Itraconazole
Griseofulvin
Terbinafide

For prolongued period of time

33
Q

What’s pityriasis versicolor?

A

A common, asymptomatic, chronic infection of the stratum corneum caused by the lipophilic yeast Malassezia furfur.
Characterised by discrete scaly depigmented areas of skin mainly on the trunk